Urinary prostaglandins are high in patients with Bartter's Syndrome - treatment with an inhibitor of prostaglandin synthesis decreased urinary prostaglandins by 80 percent, decreased plasma renin activity by 79 percent (supine) and by 76 percent (upright) and decreased urinary aldosterone by 52 percent. Potassium balance was positive and serum K ion rose with treatment in all patients. The resistance to the pressor effects of Angiotensin II and norepinephrine were restored to normal. Renal synthesis of prostaglandins is increased in Bartter's syndrome and prostaglandins mediate hyperreninemia, hyperaldosteronism and the vascular resistance to Angiotensin II and norepinephrine which characterize the syndrome.